Commission Gens ALB We fopornign v ee Foll ai Het 101 - [1940] HCA 45 - HCA 1940 case summary — Zoe

Commission Gens ALB We fopornign v ee Foll ai Het 101 - [1940] HCA 45 - HCA 1940 case summary — Zoe

[19]

"On the 6th June 1938 I was requested to fect a post-mortem examination of the body of Mr. Forst. I saw the body at the Outer Harbour in a shed adjoining a wharf. The body was lying on a hatch fully clothed. The body was dead but warm and had been dead apparently only a short while. There was a cut on the back of the left side of the head which was wet with recent blood. I saw no other external marks of violence. I was unable then to state the cause of death. I saw the body on Saturday 4th at 4.40 p.m. On Monday 6th June at the Port Adelaide Morgue I performed a post-mortem examination on the same body. That examination was done at the coroner's request. On the back of the left side of the head was a ragged cut about 1 inch long extending to the bone. Blood was evident on the scalp around this wound. There was no sign of fracture of the skull nor of internal injury to the brain nor was there any sign of cerebral haemorrhage. The heart was enlarged and showed signs of chronic valvular disease. There was atheroma of the aorta. The anterior coronary artery was blocked with a clot. This clot was not confined to the lumen. The lumen is the space of the artery. The clot was not confined to the lumen of the artery but extended through the inner lining of the vessel of the coronary artery into its wall. The other organs _ of the body were in a healthy condition and there were no other marks of violence. Death in my opinion was due to thrombosis of the coronary artery and in my opinion was sudden. Thrombosis means clotting of blood on its site. I could find no other cause of death. . . . The heart was generally enlarged especially the left ventricle. The clot that I found proceeded from an atheromatous patch. Atheroma is a fibrous disease of the inner lining of arteries which destroys their elasticity and normal distension of the vessel. Having regard to the pathological condition that I found in the coronary artery I would say that had I known that the man was suffering from symptoms and signs indicating coronary disease I

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an embolus, and that is why the blood got in under the wall. The - clot might have been an embolus. In this case in my opinion it : was not an embolus but was a thrombus. There was nothing else : that could have suggested exertion but the fracture. It was the - atheroma that caused the rupture. It predisposed the rupture, It was a weak spot. The atheromatous condition caused the clot to form on the ruptured patch. . . . Exertion could not cause the clot to form on the inner side. When once a thing was ruptured the clot would form on the other side. The exertion would not" cause the rupture to form on the inner side, that is, inside the vessel. That is the inner side of the atheromatous patch but the clot forming - on the outer side on the atheromatous patch would be due to blood coming through the wall of the vessel and this passage through the wall of the vessel would be permitted by rupture at the side of the patch and consequent passage of blood from the vessel into its wall. In this case rupture of intima may or may not have been caused by exertion. . . . This man had two thrombi, one inside and one out, but contiguous. Thrombus is not really a thrombus if it is outside the vessel. I call it a secondary thrombus. It was not sufficiently to form an aneurism on the outside of the vessel. It was a seepage through. . . . These two thrombi that I referred to were one clot extended through the intima, which is the inner lining ofthe artery. . . . Itcould have occurred as a result of exertion. s It is more likely to occur after exertion. . . . I did ane say that the pumary clot was the cause of death. The secondary clot was increasing in size and it could bulge through the wall of the vessel. The thing would be more or less continuous. The cause of the death was due to both primary and secondary thrombosis. . . . The seepage through would distend the wall of the vessel and the distention would be more towards the lumina of the vessel than the other so that you would get your blockage. I am unable to state whether the atheromatous condition did not first cause the clot to form in the lumen and then there was a seepage. through under the intima. In this particular case it is impossible to say which occurred first. By primary clot I mean the first clot and that is the one inside."

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Srevevor- limits of its capacity I mean that in normal conditions it would ai ce = perform its functions satisfactorily but if put under strain the heart Forst. may show acute insufficiency and death may follow immediately or he may not die. . . . I heard of what Forst was doing just before his death. The strain involved by that would be a heavy strain on the heart. From the description of his work I gather that he was not standing up straight but lying partly down on his abdomen. That is lying partly face downward. That would put a higher strain on the action of the heart itself. Working with his hands over his head would put an extra strain on the heart because both positions reduce the blood flow through the lungs. The fact that he was lifting the wire, he would be holding his breath during that time. I would expect some irregularity in breathing. The moment that he stops breathing the diaphragm does not move in the normal way, and the venous congestion would appear. The heart cannot fill itself properly. Another consequence is that air is not taken into the lungs and the blood is not properly oxygen- ated. The heart must therefore suffer from lack of blood and oxygen. In a normal person that would return to normal after adapting itself. If there is excess strain put on the heart it would show signs of insufficiency. First, the already decreased circulation through the lungs would decrease further more and less blood would come back from the lungs. This blood would contain little oxygen only and the coronary supply of the heart would be so little that the left ventricle might dilate and auricular fibrillation might occur. As soon as this patient would cease to work so very hard an abnormal amount of venous blood would rush to the heart and the very weak heart which did not have enough oxygen would acutely suffer from insufficiency because it had to pump this enormous amount of venous blood through the body. Then again acute insufficiency with fibrillation of the heart may occur and death follow. The blood accumulates and when breathing is resumed the blood goes to the heart and not having sufficient oxygen it is unable to do it. Having heard or read all of the evidence - the exertion done by Forst, in my opinion the cause of death was acute insufficiency of heart and lack of oxygen. This is a direct result of exertion and excess strain put on the heart. In my opinion it was not due to coronary throm- bosis. If it was due to that - I would still think that Forst's death resulted from excess strain. . . . If death was caused by thrombosis that thrombosis would have arisen through exertion

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even then one supported by the layers in the wall of coronary artery, In my opinion exertion would (not)" [sic, in transcript] "have caused that. I do not 'know of any method by which exertion could cause it to form either from inside or outside because under the stress of exertion the influences acting on that artery are of two kinds, one actually movement of the whole heart causing a possible alteration in the shape of the vessel, but as the apex of the heart and the base are relatively fixed points during contraction it is inconceivable to me that a movement of the heart is going to have any material effect in altering the shape of the vessel running directly between those two points. And two, the other influence would be a more rapid flow of blood through the coronary artery and this certainly would not be conducive to clotting. A rapid flow of blood would be less likely than a slow flow to be associated with clotting. These two points which I have raised are probably more of theoretical or hypothical interest than of practical importance and I do not believe that exercise of effort does produce coronary thrombosis which occurs so very frequently during sleep, in fact I have been called to quite as many patients suffering from the onset of coronary thrombosis during the night as during the day and hence I consider that as thrombosis can occur and frequently does so when the patient is resting it is obvious that on some occasions it must occur accident ally during the ordinary work of the day and quite irrespective of it. Coronary thrombosis. The figures vary a great deal and I could quote figures on the one hand which appear to show that professional men were much more subject to it than labourers and among recent figures including over 1,000 cases there was not shown to be much difference between labouring and professional work. After that clot had finished forming Forst's death must have occurred within a few minutes because this clot was sufficient to deprive part of the heart of its blood supply and if this had obtained at the time when he was undergoing some heavy strain I think dealing with some tackle in this case a few minutes before the death, he would most certainly have had symptoms at that time and not have gone on with the subsequent task which I believe was pulling ona rope. I say that he would have had extreme pain or breath- lessness would be the commonest but sometimes the patient would fall unconscious under those conditions practically instantaneously. I take that there was a heavy strain up on the jib and I think if there was a strain then he would have had symptoms after he had finished the milder occupation otherwise he could not have gone on with the heavier. His clot could not have been formed five minutes before. I think that with a clot of that size he would fall almost -

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thrombosis formation has been associated with the atheromatous patch, and no observations have been made on the limitation of the calibre of the vessels by the atheromatous process. I can't conceive that this patch would not be subject to any forces which might detach it. A sudden rise in pressure by expanding the distensible part of the vessel wall will tend to detach a patch from the surface. . . . If the patch were detached I would ascribe it to the steep rise of pressure extending the vessel at the time when Forst undertook the exertion. That is if this is a cause, it comes into the picture, being a rupture following a steep rise in blood pressure. Dr. Gartrell said that the patch was ruptured from the outside and not the inside. I can only say that that is astonishing news to me, that an uncomplicated atheromatous patch

by uncomplicated I mean no arteritis of the vessels - in an uncomplicated case of atheroma I am astonished to learn that such a patch is likely to be detached by breaking from vessels in the media. Atheroma is a disease of the intima and not of the media where these vessels are. And I would add in any text-book on pathology classical pictures of atheroma plates are to be seen and in none I am prepared to state this haemorrhage underneath them show part of the atheromatous process. Between the heart and the media there are two distinct surfaces. They are not related to each other. If the heart becomes loose they remain unaltered. A classical instance of involving the vessels of the media as the vessel wall as a whole is endarteritis such vessels" [sic]. '"' And then the result is an aneurism and a bulge in the vessel and the rupture of the vessel. The pressure of the blood in the vessel is almost negligible. I tried to get some measure of pressure and found that I could not give the court a figure and I came to the conclusion that it is twenty-five per cent less than in the larger vessels. The pressure in the capillaries amounting to one-fiftieth. It could only seep and form a clot provided there was some degenerated change in the media itself. And in this case I know of no such change. It is new to me. I don't accept it as very good evidence. If there were any such degenerative change as lead to bleeding from the vessels of the media it might lead to such a clot as Dr. Gartrell said he found. But in this case it would have been of such an interesting nature there would be all the more reason for keeping the vessel intact for a microscopic

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matter of testing the capacity of a heart to survive and in a H. ©. oF A. heart it can lead to fibrillation of the auricle and even to Lives th but more likely to fibrillation of the auricle and more or less 3,5: 4:pe nent increased cardiac disability. When I said defective Srevepon- wrt I meant aged or with any pathological result added it is worse. ™° £0. 1™- 'an illustration of straining effort I would mention tug of war, Fost. ning at stool when very constipated which has even caused - trying to swing the motor of an automobile when it is cold. three types of exercise or effort are all associated with holding breath and lack of other muscular movement which would bring back to the heart, and they are dangerous after a certain age. have read and heard the evidence concerning the clot. I wouldn't to say now if the clot was pre-mortal or post-mortal not having it first. If I had seen it with the naked eye I would have been by the attempt to pass probes down various vessels to see r their lumina were restricted . . . whether there was ive atheromatous restriction of the vessels because that is a wn precursor of thrombosis because it slows the circulation of the blood through those vessels and then as regards the microscopic mination it would have proved whether this clot was in fact an em clot because the structure of the clot would have been y different to a post-mortem clot. They couldn't have been d properly without microscopic examination but a person in post-mortem examinations . . . could have looked at iat clot and had no difficulty at all as an ante-mortem clot is vastly ent to a post-mortem clot in appearance. If that appearance been given in evidence I don't think I would have been here Considering the clot was ante-mortem that could have been ed by the exertion that Forst took. . . . I agree with Gartrell that the condition predisposing the clot is the slowing f the blood through the arteries. As a result of the exertion at any ze there could have been definitely a stage where a combination ing and low oxygen content of the blood could have predis- this. The low oxygen content is also a condition predisposing blood-clot formation. That could have been in consequence of exertion. In my opinion assuming that it was ante-mortem lot I think it is ignoring too great a functional disturbance occasioned this effort to say that the formation of the clot was not due to es produced by that effort. The effort in other words is noteworthy fact in relation to this cardiac death on the of the death. Assuming it was ante-mortem then it was likely the death did result from coronary thrombosis but it would be ter of dialectic at this stage but it wouldn't be incorrect. I

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from witnesses whose attainments and eminence neither could be challenged, but whose opinions exhibited no greater of unanimity than is commonly met with in other depart- ents of abstruse knowledge and of scientific research, the learned wistrate arrived at a negative conclusion. His finding was, in ubstance, that coronary thrombosis could not, in the present state { knowledge, be connected with exertion and accordingly that it not established that the workman's employment materially ributed to the cause of his death. learned judges of the Full Court considered the whole of the evidence, as, under the Act, they are entitled to do, and, g described the duty of the court to arrive at some conclusion an issue of fact, however " difficult or invidious" it might be by the state of scientific knowledge and opinion, their Honours by a course of reasoning which combined common sense the application of logic to physiological facts, to infer "on the mderance of probabilities " that the thrombus was precipitated e result, in part, of some unusual exertion undertaken by the nan before his collapse. | my opinion the conclusion of the Full Court is correct. I am ly impressed by the sequence of events. The deceased, who | arrived at an age when arterio-sclerosis and atheroma afflict |, was a stevedore's labourer. On the day of his death he ed up the jib of the crane and lay prone on the crane with his outstretched, trying to replace a wire which had come off the He failed to do so, returned to the deck and for some time, his arms in a position raised over his head, helped in holding wire rope. Immediately after performing this task he collapsed. weighs so much with me is the fact that he was brought to dstill, as an ordinary lay observer would think, by the exertion he had undergone: Cf. Partridge Jones and John Paton Ltd. r. James (1). I do not see why a court should not begin its tion, i.e., before hearing any medical testimony, from the dpoint of the presumptive inference which this sequence of ents would naturally inspire in the mind of any common-sense uninstructed in pathology. When he finds that a workman hot-so-young standing attempts in a posture calculated by the pressure on the stomach to disturb or arrest the of the heart a very strenuous task not forming part of his work and then collapses almost immediately and dies from condition, why should not a court say that here is strong d for a preliminary presumption of fact in favour of the view (1) (1933) A.C. 501, at p. 505,

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of cases now under consideration have, I think, had more detailed consideration in New Zealand than elsewhere, as is suggested by the following cases : Harvey v. B. & H. Craig Ltd. (1); Wynyard v. Daily Telegraph Co. Ltd. (2); Gwyer v. Auckland Harbour Board (3); Jarvis v. One Tree Hill Borough (4). " Until quite recently it was generally agreed that excessive physical exertion or emotion was intimately connected with the precipitation of coronary thrombi." This statement is taken from an article by Dr. J. C. Paterson in the Journal of the American Medical Association of March 1939: See also the report of Dr. Fitchett (5). And two of the medical witnesses called in the present case still, I think, adhere to it, namely, Drs. Cherry and Covernton. Medical opinion recognizes that the precipitation of coronary thrombi is not always due to effort or exertion. And many eminent men, I gather, are of opinion that effort and exertion does not contribute to and is not connected with such precipitation. Dr. Gartrell expounded this view. On the other hand, Dr. Paterson in his paper suggests that high coronary blood pressure, the result of strenuous exercise or of emotion (or of persistent hypertension), is one of the underlying causes of capillary rupture and intimal haemorrhage in arterio- sclerotic coronary arteries. If conditions are favourable, he suggests that the various changes which result from capillary rupture may then be the initiating factors in the disposition of coronary thrombi. He thus summarizes his views and conclusions : - ' The formation of coronary thrombi is a gradual process, sometimes occupying several days before occlusion of the coronary lumen, with its resultant cardiac pain, is produced. Therefore the activities of a patient immediately preceding the onset of an attack of coronary thrombosis have no relation to the etiology of the precipitation of a thrombus but are purely coincidental. The pathologic appearance in a series of fatal cases of coronary thrombosis suggests strongly that excessive exercise and emotional stress are intimately concerned in the mechanism of coronary artery thrombosis." Both Professors Cleland and Hicks of the Adelaide University were impressed, I think, with this theory. Another theory may be found in the report of Dr. Fitchett (6), that effort or exertion provoke a demand from the heart for extra blood, which defective coronary arteries cannot supply, thus inducing a relative ischaemia and exciting ventricular fibrillation which leads in a material degree - to a fatal issue. But, in all this uncertainty, there is a passage -

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as far as he could see, that the evidence of the times in which such cases occurred did not seem to associate the onset with effort and 'that the impression was (and it was mentioned to students) that coronary thrombosis does not seem to be related to effort. In reference to this statement, their Honours say : " It may be difficult for us to draw an inference that medical men hesitate to draw, but we do not think that we can refuse to enter upon an inquiry because _ it is difficult or invidious, and it seems to us that Professor Cleland has given us the material for a conclusion." The judgment then sets out a course of reasoning of a medical nature, some of the materials for which are drawn from contributions to medical literature that were in evidence and contained an exposition which Professor Cleland appeared to their Honours to accept. After citing a passage from Professor Cleland's evidence, the judgment continues as follows : - "' We agree with the witness that, speaking generally, it must be difficult and probably impossible to relate an attack of coronary thrombosis to any particular activity of the patient, and we concede that, even in this case, it is difficult to feel any great confidence in the inference, but it seems to us that we have here

the coincidence of strenuous physical exertion occurring at or about the time when the thrombus must have commenced to precipitate. If the expert evidence shows, as we think it does, that physical effort is commonly - though not invariably - the inciting cause of that phenomenon, we think we are entitled to draw the inference that Professor Cleland felt unable to draw. We fully accept his view that the evidence is in some measure inconclusive. For the purposes of a scientific deduction it may be insufficient, but we 'Tepeat that courts of justice are entitled and bound to act upon the probabilities of the case." The difficulty I feel in adopting these 'views lies in three considerations. __ First, I think that upon a question of fact of a medical or scientific description a court can only say that the burden of proof has not been discharged where, upon the evidence, it appears that the _ present state of knowledge does not admit of an affirmative answer and that competent and trustworthy expert opinion regards an affirmative answer as lacking justification, either as a probable inference or as an accepted hypothesis.